ELECTROPHYSIOLOGICAL EVIDENCE FOR GLUTAMATE AS A VOMERONASAL RECEPTORCELL NEUROTRANSMITTER

Authors
Citation
Ca. Dudley et Rl. Moss, ELECTROPHYSIOLOGICAL EVIDENCE FOR GLUTAMATE AS A VOMERONASAL RECEPTORCELL NEUROTRANSMITTER, Brain research, 675(1-2), 1995, pp. 208-214
Citations number
17
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
675
Issue
1-2
Year of publication
1995
Pages
208 - 214
Database
ISI
SICI code
0006-8993(1995)675:1-2<208:EEFGAA>2.0.ZU;2-M
Abstract
Bipolar receptor cells in the vomeronasal organ send axonal projection s to the accessory olfactory bulb where they synapse with mitral cell dendrites. Although the nature of the synapse is thought to be excitat ory, the neurotransmitter(s) involved has not yet been identified. Ele ctrophysiological recordings of single neurons in the mitral cell laye r of the AOB in response to vomeronasal nerve stimulation were conduct ed to characterize the synaptic response and the underlying neurotrans mitter substance. Extracellular activity was recorded in vivo (whole a nimal) and in vitro (AOB slice) from female rats. In vivo, the predomi nant response to stimulation of the VNO was excitation. In many instan ces in the whole animal preparation, the excitation was followed by an inhibitory response. Attempts to block the excitatory response by eje cting kynurenic acid in close proximity to the mitral cell being recor ded were not successful. Since this failure may have been due to inabi lity of the antagonist to reach its presumed site of action at the den drite, further recordings were carried out in vitro. In the AOB slice preparation, the predominant response to stimulation of the VN nerve e ndings was excitation. Superfusion of the non-NMDA antagonist, CNQX, i nto the medium resulted in a reduction of the orthodromic excitation i n 5 of 8 cells. The NMDA antagonist, AP-5, was found to blunt orthodro mic excitation in 1 of 4 cells. These results suggest that the excitat ory response evoked in mitral cells following stimulation of the VN ne rve is mediated by glutamate.